Use of CT Imaging and Three-Dimensional Color Reconstruction for Comparison of Cranial Anatomy and Density in Captive and Wild Cheetahs (Acinonyx jubatus)
American Association of Zoo Veterinarians Conference 1997
Christine V. Fiorello1, MS; David A. Fagan2, DDS; James E. Oosterhuis3, DVM; Helena Fitch-Snyder; Janet E. Fagan2
1School of Veterinary Medicine, Tufts University, North Grafton, MA, USA; 2The Colyer Institute, San Diego, CA, USA; 3Zoological Society of San Diego, San Diego, CA, USA


Cheetahs are declining in the wild and do not prosper in captivity.2,3 They have notoriously low fertility and high infant mortality in captivity.2,4 Though it is tempting to attribute their problems to low genetic diversity, disorders caused by husbandry must not be ignored, as these are more likely to be prevented. In 1982 Fitch and Fagan described a condition in captive cheetahs called focal palatine erosion (FPE).1 The etiology of the disorder remains unknown, though it has been suggested that it is a disease of captivity and thus environmental, not genetic, causes.1,5 The hypothesis put forth by Fitch and Fagan explained the condition as a defect in occlusion of the molars, caused by lack of the “hassle factor” during development. The “hassle factor” is absent in captive raised animals because they are fed soft commercial diets, and thus are not exercising their masticatory apparatus by manipulating tendons, ligaments, and bone. Affected animals have clinical signs of dysphagia and osteomyelitis, and on physical examination they have a defect in the hard palate caused by traumatic insult by the lower molar. To further investigate this disorder, we scanned seven skulls using computed tomography technology and three-dimensional color reconstruction. We looked at two skulls from wild cheetahs killed in Kenya in 1910, two skulls from captive cheetahs at the San Diego Wild Animal Park who died in the 1980s, and three skulls from wild cheetahs killed in Namibia in the 1990s. Preliminary results showed that all the wild cheetahs examined have greater bone density through their skulls when compared to the captive animals. If this is the case, it suggests that FPE is not an isolated problem of occlusion, but a generalized disorder of the skeletal components of the head. We are hypothesizing that lack of the “hassle factor” causes a failure of adequate development of the bony elements of the jaws. Because the size of the teeth is determined prenatally and not influenced by diet, the teeth are too large for the underdeveloped jaw and malocclusion results. In addition, the bones are not stressed sufficiently, leading to less mineral deposition and thus lower density. The malocclusion is the immediate cause of the trauma to the hard palate, but the lesions are exacerbated by the poor bone density. If this hypothesis is correct, it is likely that altering the diet of young cheetahs in captivity would prevent FPE and its associated morbidity and mortality.

Literature Cited

1.  Fitch HM, Fagan DA. 1982. Focal palatine erosion associated with dental malocclusion in captive cheetahs. Zoo Biology 1: 295–310.

2.  Marker-Kraus L, Grisham J. 1993. Captive breeding of cheetahs in North American zoos (1987–1991). Zoo Biology 12: 5–18.

3.  Marker-Kraus L, Kraus D, Barnett D, Hurlbut S. 1996. Cheetah survival on Namibian farmlands. USAID Environmental Education Project, Windhoek, Namibia.

4.  O’Brien SJ, Roelke ME, Marker L, Newman A, Winkler CA, Meltzer D, Colly L, Evermann JF, Bush M, Wildt DE. 1985. Genetic basis for species vulnerability in the cheetah. Science 227: 1428–34.

5.  Phillips JA, Worley MB, Morsbach D, Williams TM. 1993. Relationship among diet, growth, and occurrence of focal palatine erosion in wild-caught captive cheetahs. Madoqua 18 (2): 79–83.


Speaker Information
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Christine V. Fiorello, MS
School of Veterinary Medicine
Tufts University
North Grafton, MA, USA

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